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Dissecting corollary discharge dysfunction in schizophrenia

Authors

  • Judith M. Ford,

    1. Psychiatry Service, Veterans Affairs Connecticut Healthcare System, West Haven, Connecticut, USA
    2. Department of Psychiatry, Yale University School of Medicine, New Haven, Connecticut, USA
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  • Max Gray,

    1. Psychiatry Service, Veterans Affairs Palo Alto Health Care System, Palo Alto, California, USA
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  • William O. Faustman,

    1. Psychiatry Service, Veterans Affairs Palo Alto Health Care System, Palo Alto, California, USA
    2. Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, California, USA
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  • Brian J. Roach,

    1. Psychiatry Service, Veterans Affairs Connecticut Healthcare System, West Haven, Connecticut, USA
    2. Department of Psychiatry, Yale University School of Medicine, New Haven, Connecticut, USA
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  • Daniel H. Mathalon

    1. Psychiatry Service, Veterans Affairs Connecticut Healthcare System, West Haven, Connecticut, USA
    2. Department of Psychiatry, Yale University School of Medicine, New Haven, Connecticut, USA
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  • This work was supported by the VA Schizophrenia Biological Research Center and grants from National Institute of Mental Health (MH40052, MH 58262, MH067967) and the National Alliance for Research in Schizophrenia and Affective Disorders (NARSAD). We thank Drs. Alison Adcock and Sophia Vinogradov for referring patients to this study.

Address reprint requests to: Judith M. Ford, Ph.D., Department of Psychiatry, Yale University School of Medicine, 950 Campbell Ave., VA CT Healthcare System, 116A, West Haven, CT 06517, USA. E-mail: Judith.ford@yale.edu

Abstract

During talking, a corollary discharge prepares cortex for self-generated sounds, minimizing responsiveness and providing a way to recognize sounds as self-generated. When we talk, we are the agent producing the sound and know what sound to expect. The auditory ERP N1 is normally suppressed during talking, but less so in schizophrenia, perhaps due to deficits in agency and expectancy inherent to talking. N1 was assessed in 27 patients (23 schizophrenia, 4 schizoaffective) and 26 controls. During talking, subjects said “ah” every 1–2 s. During agency, subjects pressed a button to deliver “ah” every 1–2 s. During expectancy, “ah” followed a visual warning. Talking yielded greatest N1 suppression in controls and greatest suppression failure in patients. Agency and expectancy had modest suppression effects on N1 and only in controls. Group differences in expectancy and agency could not account for failed corollary discharge during talking in patients.

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